Calcific aortic valve stenosis (AVS) is the most frequent heart valve disorder. The culprit disease process of AVS is the progressive mineralization of the aortic valve, including the aortic valve cusps, annulus, and root. The incidence of this disease increases with age, hypertension, diabetes, dyslipidemia, and is often associated with a bicuspid aortic valve, a congenital abnormality present in 1-2% of the population. AVS is a slow and progressive disorder that can be diagnosed at an early stage with the use of cardiac auscultation and Doppler-echocardiography. This disease pattern thus provides a relatively long time window of opportunity, during which patients might be treated by pharmacologic agents before mineralization of the valve becomes too extensive and causes a severe obstruction to left ventricular outflow tract. Unfortunately, there is currently no medical treatment available to prevent the development and progression of this disease and aortic valve replacement surgery remains the only efficient treatment when AVS becomes severe.
Calcification of the aortic valve is an intricate process involving a balance between promoting and anti-calcifying mechanisms. In this regard, expression of ectonucleotidase enzymes may modulate calcification of the aortic valve. Among those enzymes, ectonucleotide pyrophosphatase/phosphodiesterases (ENPPs), ectonucleoside triphosphate diphosphohydrolases (ENTPDs), and 5′-nucleotidase (NT5E) use nucleotides as substrate and may modulate mineralization. The presence and regulation of these enzymes has never been studied in aortic stenotic (AS) valves.